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Gene-environment Interaction Models to Unmask Susceptibility Mechanisms in Parkinson's Disease
Published on: January 7, 2014
Susceptibility to a parkinsonian toxin varies during primate development
B A Morrow1, R H Roth, D E Redmond
1Neuropsychopharmacology Research Laboratory, Department of Psychiatry, Yale University School of Medicine, New Haven, CT 06511, USA.
Experimental Neurology
|February 28, 2012
Summary
Developing dopamine neurons are vulnerable to toxins during primate mid-gestation. This suggests a heightened risk from environmental exposures during fetal development, potentially impacting Parkinson's disease later in life.
Area of Science:
- Neuroscience
- Developmental Biology
- Toxicology
Background:
- Parkinson's disease involves nigrostriatal dopamine neuron loss, exceeding normal aging effects.
- Early developmental stages are hypothesized as vulnerable periods for dopamine neuron compromise.
- Environmental or genetic factors may impact dopamine neuron development and long-term health.
Purpose of the Study:
- To investigate the developmental vulnerability of primate nigrostriatal dopamine neurons to a parkinsonian neurotoxin.
- To determine if MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) affects dopamine neurons differently across developmental stages.
Main Methods:
- Utilized the neurotoxin MPTP to assess dopamine neuron vulnerability at various primate developmental stages.
- Measured dopamine, homovanillic acid, 1-methyl-pyridinium, and tyrosine hydroxylase immunoreactivity.
Main Results:
- Dopamine neurons showed relative vulnerability to MPTP during mid-gestation.
- Neurons were resistant to MPTP later in development and in young primates.
- MPTP exposure revealed differential susceptibility based on developmental timing.
Conclusions:
- Mid-gestation exposure to environmental agents causing oxidative stress poses a significant risk to fetal dopamine neurons.
- Uncoupling protein-2 may be a therapeutic target to mitigate dopamine neuron loss in Parkinson's disease and aging.
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